synovitis/nicotine

Stimulation of the cholinergic inflammatory pathway can attenuate collagen-induced arthritis (CIA) and inhibit synovitis by Janus kinase (JAK) 2 and signal transducer and activator of transcription (STAT) 3 signaling. Suppressor of cytokine signaling (SOCS) protein can also regulate the inflammatory

Mycoplasma synoviae was isolated from the trachea of chickens showing either typical infectious synovitis lesions or air-sacculitis. M. synoviae was identified by means of the direct plate fluorescent antibody technique and its growth-dependence on nicotine-amide-adenine dinucleotide. This is the

Rheumatoid arthritis is an autoimmune disease characterized by the production of two known antibodies - rheumatoid factor and anti-citrullinated peptide antibody (ACPA) - against common autoantigens that are widely expressed within and outside the joints. The interactions between genes and

Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease characterized by extensive synovitis resulting in erosions of articular cartilage and marginal bone with joint destruction. The lack of immunological tolerance in RA represents the first step toward the development of autoimmunity.

Rheumatoid arthritis (RA) is progressive, chronic, autoimmune, systemic connective tissue disease. It affects 0,5-1% population. RA manifests as inflammation of symmetrical mainly small and medium joints with synovial hypertrophy, extra-articular lesions and systemic complications. Depending on

A 28-year-old African American male with a history of synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome, tobacco use, and sickle cell trait was referred to a physiatrist at a multidisciplinary spine center with a one-year history of non-traumatic thoracic back pain that had

RA is a complex multifactorial chronic disease that transitions through several stages. Multiple studies now support that there is a prolonged phase in early RA development during which there is serum elevation of RA-related autoantibodies including RF and ACPAs in the absence of clinically evident

Multiple genetic and environmental factors have been associated with an increased risk for rheumatoid arthritis (RA). Of these, the strongest associations have been seen with female sex, a family history of RA, the genetic factor the "shared epitope," and exposure to tobacco smoke. There is also